Evidence map›Paper›PMID 22128300›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012

Loss of 18q22.3 involving the carboxypeptidase of glutamate-like gene is associated with poor prognosis in resected pancreatic cancer.

Jih-Hsiang Lee, Elisa Giovannetti, Jin-Hyeok Hwang, Iacopo Petrini, Qiuyan Wang, Johannes Voortman, Yonghong Wang, Seth M Steinberg, Niccola Funel, Paul S Meltzer and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Role of CYB5A in pancreatic cancer prognosis and autophagy modulation.Journal of the National Cancer Institute · 2014
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 4 countries.

Jih-Hsiang LeeMedical Oncology Branch, Genetic Branch, and Biostatistics and Data Management Section, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Elisa Giovannetti
Jin-Hyeok Hwang
Iacopo Petrini
Qiuyan Wang
Johannes Voortman
Yonghong Wang
Seth M Steinberg
Niccola Funel
Paul S Meltzer
Yisong Wang
Giuseppe Giaccone
Data Management (Italy) · ITAmsterdam UMC Location Vrije Universiteit Amsterdam · NLNational Cancer Institute · USUniversity of Pisa · ITSeoul National University Bundang Hospital · KR

Funding

Office of Collaborative BiostatisticsZIDSC007202 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI CHOO-WOSOBA, HYOYOUNG · 2009 to 2025
$14.5M
Thorarcic Cancer Research LaboratoryZIABC011269 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GIACCONE, GIUSEPPE · 2010 to 2013
$5.4M
Intramural NIH HHS ZIA BC011269
6 · The paper itself

Abstract

purposesPancreatic cancer is the fourth leading cause of cancer-related death, and studies on the clinical relevance of its genomic imbalances are warranted. EXPERIMENTAL

designRecurrent copy number alterations of cytobands and genes were analyzed by array comparative genomic hybridization (aCGH) in 44 resected pancreatic cancer specimens. Prognostic markers identified by aCGH were validated by PCR gene copy number assay in an independent validation cohort of 61 resected pancreatic cancers. The functions of gene identified were evaluated by proliferation, cell cycle, and migration assays in pancreatic cancer cells.

resultsWe showed recurrent copy number gains and losses in the first cohort. Loss of 18q22.3 was significantly associated with short-term overall survival in the first cohort (P = 0.019). This cytoband includes the carboxypeptidase of glutamate-like (CPGL) gene. CPGL gene deletion was associated with shorter overall survival in the validation cohort (P = 0.003). CPGL deletion and mutations of TP53 or Kras seem to be independent events. A Cox model analysis of the two cohorts combined showed that loss of 18q22.3/deletion of the CPGL gene was an independent poor prognostic factor for overall survival (HR = 2.72, P = 0.0007). Reconstitution of CPGL or its splicing variant CPGL-B into CPGL-negative pancreatic cancer cells attenuated cell growth, migration, and induced G(1) accumulation.

conclusionLoss of 18q22.3/deletion of the CPGL gene is a poor prognostic marker in resected pancreatic cancer, and functional studies suggest the CPGL gene as growth suppressor gene in pancreatic cancer.

Indexed as

Chromosome DeletionAgedAged, 80 and overCarcinoma, Pancreatic DuctalCell Line, TumorChromosomes, Human, Pair 18Cohort StudiesComparative Genomic HybridizationDipeptidasesDisease-Free SurvivalDNA Copy Number VariationsDNA Mutational AnalysisFemaleGenes, Tumor SuppressorHumansKaplan-Meier EstimateCNDP2 protein, humanDipeptidasesKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID22128300
PMCPMC3261299
OpenAlexW2045633623

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.